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Physio Sem 2 Exam 3 (Voltz) > Endocrine - Pathophysiologies > Flashcards

Endocrine - Pathophysiologies Flashcards

1
Q

Compare the speed and magnitude of effects between the endocrine system and the CNS.

A

CNS effects are specific, immediate, and direct (exerted by cell APs).

Endocrine system effects are slower, cascade-like (global/multi-system effects), and dependent on indirect feedback mechanisms for tight autoregulation.

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2
Q

The thyroid gland is well vascularized. T/F?

A

True.

This allows the hormones it releases to circulate efficiently and directly into the bloodstream.

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3
Q

Where is the thyroid gland? Briefly describe its appearance.

A

The thyroid gland covers the cricoid cartilage.

It is a bilobar structure connected in the middle.

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4
Q

Why are thyroid goiters a concern to our airway management?

A

They can cause tracheal deviations, press on laryngeal nerves, and can completely engulf the trachea.

They can also cause tracheal erosion or tracheal malacia (softening of tracheal tissues from constant pressure).

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5
Q

Describe the release of thyroid hormones.

A
  1. Thyroid gland is filled by globular structures (thyroglobulin) composed of thyroid hormones incorpoated into big chains (globulin)
  2. Thyroid hormones (T3/T4) are cleaved off the globulin chains when they are needed.
  3. T3 and T4 bind to Thyroxine-Binding Globulin (a carrier protein) and are subsequently released into the bloodstream.
  4. T4 is converted to T3 via extra-thyroidal de-iodination in serum. T3 is primarily responsible for most thyroid hormone effects.
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6
Q

What is the role of iodine in thyroid hormone function?

A

Iodine from the GI tract is incorporated into T3 and T4 for synthesis of their active forms for serum circulation.

It is incorporated into the Thyroid Hormone-Globulin complex that is released to the circulation.

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7
Q

What is the effect of iodine deficiency on thyroid hormone function?

A

T3 and T4 active forms require iodine so without iodine, they cannot exert their effects.

As a result, thyroid hormone keeps getting produced in excess due to the lack of negative feedback to the hypothalamus and anterior pituitary (TRH, TSH). This results in the masses you see in thyroid goiters.

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8
Q

Describe the regulation of thyroid hormones.

A

Hypothalamus releases TRH (thyrotropine releasing hormone).

TRH stimulates anterior pituitary to release TSH (throid stimulating hormone).

TSH cleaves T3 and T4 from their globulin chains (activation and release) and increased production of thyroglobulins.

T3 and iodine provide negative feedback mechanism to hypothalamus and anterior pituitary.

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9
Q

What are some iatrogenic causes of hypothyroidism?

A

DIrect surgical damage to the thyroid.

Accumulation of radioactive iodine from radiation therapy or imaging procedures.

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10
Q

What are functions of thyroid hormone?

A

Increases carbohydrate and fat metabolism.

Increases body’s metabolic rate.

Important for growth.

Important for stress response.

Increases adrenergic-receptor sensitivity.

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11
Q

How do thyroid hormones exert their effects at the cellular level?

What are the clinical implications of this?

A

They make their way to the nucleus of the cell, increase production of certain porteins through selective RNA/DNA upregulation (gene transcription)

**Works slowly over the course of days and weeks.

Clinically, this means that it takes time for thyroid dysfx to induce noticeable problems and it takes time to correct thyroid dysfx.

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12
Q

Thyroid hormones are extensively protein bound. T/F?

A

True

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13
Q

What are two patient conditions that can cause increased T3/T4 function in the serum?

A

Anemia (more free T3/T4)

Acidemia (disruption of T3/T4 protein binding)

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14
Q

What are symptoms of hyperthyroidism?

A

Sweating

Heat intolerance

Neurotic anxiety

Muscle weakness (prolonged NMB)

Fine tremor

Brisk reflexes

Diarrhea

Wt loss despite increased appetite

Osteoperosis

A-fib

Strong, rapid pulse

Wide pulse pressure

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15
Q

What are some primary causes of hyperthyroidism?

A

Grave’s Disease (antibodies react to thyroid, leading to unregulated release of T3/T4)

Hashimoto’s thyroiditis (autoimmune destruction of thyroid gland; initial large release of T3/T4 sequestered in the thyroid gland followed by eventual hypothyroid state due to lack of T3/T4 production)

Hot adenoma (thyroid gland tumor that results in unregulated T3/T4 production)

Fictitious (pt takes too much exogenous thyroid hormones)

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16
Q

What are some secondary causes of hyperthyroidism?

A

Pituitary adenoma

Hypothalamic derangements

Ectopic TSH secretion

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17
Q

What are cardiac effects of hyperthyroidism?

A

Tachycardia

A-fib

CHF

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18
Q

What are some treatment options for hyperthyroidism?

A

Inhibit synthesis (PTU, methimazole)

Inhibit release (KI, NaI)

Block end results (beta-blockers)

Propranalol = first line intra-op treatment for thyroid storm as are other beta blockers (other treatments take time or have a rebound effect)

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19
Q

How should hyperthyroid patients be managed pre-operatively?

A

If case is elective, patient should be euthyroid (normalize TFT, HR < 85, continue medications on day of surgery).

If case is emergent, control their hyperdynamic state with anesthetics.

TFT - thyroid function tests

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20
Q

What are some anesthetic considerations with hyperthyroidism?

A

Protect eyes (may be bulging, esp in Graves)

Closely monitor CV

Accurate temp monitoring

Avoid sympathetic stimulating drugs (ketamine, pancuronium)

Pt likely hypovolemic and vasodilated

Careful with muscle relaxants (may last a long time)

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21
Q

What is thyroid storm an end result of?

A

Unregulated hyperthyroid state that has progressed significantly beyond patient’s autoregulatory controls

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22
Q

Which other intra-operative condition can thyroid storm resemble?

A

malignant hyperthermia

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23
Q

What are some symptoms of thyroid storm?

A

Hyperpyrexia

Tachycardia

Mental status changes

HoTN due to CV collapse/hypovolemia

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24
Q

When does thyroid storm most commonly occur?

A

6-24 hours post-op

(it can still occur itnra-op though)

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25
Q

Although thyroid storm can mimic MH, what are two key effects that MH has but thyroid storm does not mimic?

A

Thyroid storm = no muscle rigidity, no lactic acidosis

Note: patient can still become acidotic from other means

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26
Q

How should we treat thyroid storm?

A

Volume replacement

CV control

Block thyroid hormone release

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27
Q

What are symptoms of hypothyroidism?

A

Slowing of mind and body

Hair thinning

Depression/irritability (mental status changes)

Big tongue

Croaky voice (laryngeal collapse)

Dry, cold skin

Cold intolerance

Constipation

High LDL

Slow reflexes

Weak pulse

Myxedema (global swelling of the body)

Inability to regulate BP due to low catecholamine response

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28
Q

Goiter can develop in both hypo and hyperthyroid patients. T/F?

A

True

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29
Q

How can goiters lead to stridor? What are the anesthetic implications of this?

A

Goiters can damage laryngeal nerves and disrupt vocal cord innervation.

This leads to stridor.

Anesthetic implication: patient may be unable to protect airway after extubation.

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30
Q

What is myxedema coma a result of? What is it characterized by?

A

Result of uncontrolled hypothyroidism

It is characterized by cells being almost completely dysfunctional due to lack of metabolic stimulus (pt cannot support him/herself)

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31
Q

Why are hematomas and pneumothoraces a risk of thyroid surgery?

A

Removal of a goiter can result in bleeding into the lungs or hematomas.

Pneumothoraces can also occur since the thyroid and/or goiter may extend down close to the lungs behind the sternum. (and surgeon will need to operate there)

32
Q

What is tracheal malacia?

A

Thinning of the trachea.

May lead to tracheal collapse since it gets weaker and less able to support itself.

Goiters can cause this.

33
Q

Describe where adrenal glands are and what they look like briefly.

A

They are located in the retroperitoneal space on top of both kidneys.

They look like pyramid-shaped fatty tissue glands that sit on top of the kidneys bilaterally.

34
Q

Describe the pathway of cortisol release.

A

CRH (hypothalamus) –> ACTH (ant pituitary gland) –> ACTH circulates in blood stream –> Adrenal Cx hormones including cortisol

CRH - corticotropin releasing hormone

35
Q

Describe the negative feedback that allows tight regulation of the stress response (Cortisol).

A

Circulating cortisol inhibits ACTH release from the ant pituitary

ACTH inhibits CRH release from the hypothalamus

36
Q

The adrenal medulla covers the adrenal cortex. T/F?

A

False; the adrenal cortex covers the adrenal medulla which forms the center of the adrenal gland.

37
Q

What is the function of the adrenal medulla?

A

Production of catecholamines (epinephrine, NE, dopamine)

38
Q

What is the function of the adrenal cortex?

A

It is responsible for the synthesis and release of multiple steroid hormones including cortisol, aldosterone, and androgens (sex hormones).

(These hormones are produced in discrete layers of the adrenal Cx: mineralocroticoid, glucocorticoid, and androgen strips)

39
Q

What is the molecular basis of steroid hormones?

A

Cholesterol

40
Q

What is the function of aldosterone and how does it work?

A

Aldosterone regulates fluid and electrolyte blanace by increasing Na+ reabsorption from the distal tubules of the kidneys.

This leads to retention of water (passively follows Na+)

Na+ reabsorption is increased by aldosterone-mediated production of Na+ protein channels.

41
Q

How is the aldosterone system regulated?

A

It is regulated by the RAA system.

ACTH stimulates both the RAA system and cortisol production.

The RAA system is stimulated by hypotensive states: Renin converts angiotensinogen to antiotensin 1 which is released into the bloodstream. Angiotensin 1 gets converted to angiotensin 2 in the lungs via ACE.

42
Q

Compare the function of angiotensin 1 and angiotensin 2.

A

Angiotensin 1 mainly functions as a precursor to angiotensin 2.

Angiotensin 1 is far less potent in causing sodium reabsorption than angiotensin 2 and does not cause aldosterone release.

43
Q

What is renal vasculature hypotension? What does it result in?

A

Hypoperfusion of the kidneys caused by narrowing of the renal artery.

This is sensed as a HoTN state and will activate the RAA system.

44
Q

What is the primary effect of low glucocorticoids level in the context of surgical stimulation?

A

Low levels cause low smooth muscle response to inotropic and vasopressor actions of catecholamines (and therefore many of our pressor drugs)

45
Q

High levels of glucocorticoids can cause Na+ excretion and water loss. T/F?

A

False. High levels cause Na+ and water retention.

This is most likely secondary to concurrent ACTH stimulation of aldosterone.

46
Q

What is the effect of glucocorticoids on glucose in our body?

A

It causes hyperglycemia.

Utilization of glucose outside of the liver is decreased for redirection to our brain cells.

Overall effect = hepatic stores of glucose are preserved and glucose utilization in tissues (esp the brain) are increased.

47
Q

What are the side effects of hyperproduction of androgens?

A

Overexpression of secondary sex characteristics

Abnormal function of muscle cells

Cardiotoxicity

Neural effects with chronic use/oversynthesis

48
Q

What is pheochromocytoma?

A

A state of catecholaminergic overload due to tumor(s) on or near the adrenal gland.

49
Q

What are symptoms of pheochromocytoma?

A

HTN (rare)

Paroxysmal headache

Sweating

Palpiations

Tachycardia

Wt loss

Heat intolerance

50
Q

What is pheochromocytoma usually caused by?

A

Tumors in the adrenal medulla that stimulate overproduction of catecholamines.

51
Q

What are less common causes of pheochromocytoma?

A

Tumors along the sympathetic chain (outside if the adrenal medulla).

Anywhere where there are neuroblast cells (they function as progenitors for sympathetic cells)

52
Q

What are the results of stimulating A1 and A2 adrenergic receptors?

A

Alpha 1: vasoconstriction, intestinal relaxation, uterine contraction, pupillary dilation

Alpha 2: vasoconstriction, decreased presynaptic NE, platelet aggregation, decreased insulin secretion

53
Q

What are the effects of stimulating beta adrenergic receptors?

A

B1: Increased HR/contractility, lipolysis, renin secretion

B2: vasodilation, bronchodilation, increased glycogenolysis

B3: increased lipolysis and brown fat thermogenesis

54
Q

How should pheocromocytoma be managed pre-operatively?

A

Adrenergic blockade (alpha then beta blocks) to control resting blood pressures, HR, heart ryhthms, and coronary blood flow

Fluid replacement

55
Q

How should pheochromocytoma be managed intra-operatively?

A

Control systemic pressures with alpha blockade (phenoxybenzamine, phentolamine, SNP, nicardipine) and beta blockade

Large bore IV acess for fluid shifts (we may have to play catch-up after tumor excision as catechole levels drop)

Avoid sympathetic stimulants (hypoventilation, ephedrine, ketamine, pancuronium, halothane)

56
Q

During operation for a pheochromocytoma tumor, we often see significant HoTN following the tumor excision.

What are the three most common reasons for this?

A

Cessation of catecholamine synthesis and release due to tumor excision

Excess treatment of HTN state before tumor excision

Inadequate fluid resuscitation

57
Q

What are two common causes of excess cortisol?

A

Aldosteronoma

Cushing’s Syndrome

58
Q

What is a common cause of too little cortisol?

A

Addison’s disease

59
Q

What causes aldosteronoma?

A

Tumors directly on adrenals that causes too much hormone release or on hypothalamus/pituitary that causes too much ACTH release

60
Q

What is Conn’s syndrome?

A

A type of primary aldosteronoma characterized by hyperaldosteronism.

Due to lack of regulation by negative feedback mechanisms

61
Q

What are symptoms of aldosteronoma?

A

Excessive aldosterone release (main issue)

Increased BP

Hypervolemia (spironolactone = great treatment)

Hypokalemia

Muscle weakness

Metabolic alkalosis (secondary to renal proton wasting)

[hypokalemic metabolic alkalosis]

62
Q

What is Cushing’s syndrome?

A

A common hyperadrenal state primarily due to tumors but can also be seen with exogenous intake of steroids.

63
Q

What are symptoms of Cushing’s Syndrome?

A

Muscle wasting (leads to muscle weakness, caution with NMBs)

Osteoperosis

Central obesity (includes fat deposition on face and upper back - moon face and buffalo hump)

Abdominal Striae

Glucose intolerance

HTN

Mental status changes

64
Q

What is the most common causes of primary Cushing’s syndrome?

A

Pituitary tumor that leads to hypersecretion of ACTH (unresponsive to negative feedback from serum cortisol levels

Adrenal tumor that leads to direct hypersecretion of c)ortisol from adrenal (unresponsive to negative feedback from cortical structures)

65
Q

What is a method that we can use to differentiate between primary and secondary Cushing’s syndrome?

A

Secondary Cushing’s syndrome = due to something outside of the HPA axis

We can administer Decadron to the patient and check the levels of serum cortisol the next morning.

If it is primary Cushing’s syndrome, cortisol levels will remain high due to dysfx of adrenal regulation. If it is secondary Cushing’s syndrome, cortisol levels will hav edropped due to intact HPA system regulation.

66
Q

60-70% of patients with Cushing’s syndrom present with a pituitary tumor that is the cause of the dysfx. T/F?

A

True

67
Q

What is a common procedure performed to correct Cushing’s syndrome?

A

Trans-sphenoidal pituitary resection (minimally invasive)

68
Q

What populations of patients are at higher risk for Cushing’s syndrome?

A

Patients that have been in the ICU for a long time

Patients that are on chronic steroids

Patients that have received multiple etomidate doses (esp in trauma)

69
Q

What are some anesthetic conerns we would have about patients with Cushing’s syndrome?

A

Fluid overloaded state (due to high aldosterone)

Hypokalemia (leads to muscle weakness & wasting)

Metabolic acidosis

Higher risk for fractures

Muscle weakness leading to prolonged paralysis

Stress intolerance requiring stress dose of steroids

70
Q

What is Addison’s disease and what are two common causes?

A

Addison’s disease: destrucion of the adrenal gland

Common causes: auto-immune reaction and hemorrhage into the adrenal gland (esp in anti-coagulated patients)

71
Q

What is the primary cause of Addison’s disease symptoms?

A

Destruction of cortisol and aldosterone synthesis

72
Q

In patients that are hyperkalemic but present without renal issues, what do we have to rule out?

A

Adrenal insufficiency and hypoaldosterone

73
Q

What are four symptoms that we see in Addison’s patients in the OR?

A

Hyponatremia

Hyperkalemia

HoTN

Wt loss

Poor stress response

74
Q

Your patient seems hypovolemic and is not responding well to your pressors or fluid boluses. What do you need to rule out as a primary cause?

A

Adrenal insufficiency

75
Q

5 mg predisone = ___ mg hydrocortisone = ___ mg methylprdnisolone = ___ decadron = ____ cortisone acitate

A

20

4

6

25

Physio Sem 2 Exam 3 (Voltz) (2 decks)

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